Diarrhea, PPI Use, and Pain in a Restaurant Worker From Mexico

Jaimy Villavicencio Kim, MD; John W. Birk, MD


November 18, 2022

H pylori infection is the most common chronic bacterial infection worldwide.[8] Its prevalence is closely related to low socioeconomic status and unsanitary living conditions during childhood, which is when the infection is most commonly acquired.[8,9] Transmission is thought to occur via the oral-oral route or the fecal-oral route or from contaminated water. It is estimated that patients with H pylori infection have a 10%-20% lifetime risk for peptic ulcer disease and a 1%-2% risk for gastric cancer.[9] Other diseases associated with H pylori infection include mucosa-associated lymphoid tissue (MALT) B cell lymphoma and immune thrombocytopenic purpura.[10]

The different clinical presentations of H pylori infection include dyspepsia, peptic ulcer disease (Figure 2), gastric adenocarcinoma, and gastric lymphoma. Peptic ulcer disease most commonly presents with symptoms similar to those of dyspepsia: abdominal pain, nausea, vomiting, and early satiety. If peptic ulcer disease is severe, perforation, bleeding, and gastric outlet obstruction/pyloric stenosis can occur.[8] An association with diarrhea has not been well established, but the resolution of diarrhea after treatment has been reported, especially in infants.[11]H pylori infection is also a risk factor for colonic polyps.[12]

Figure 2.

In patients with H pylori infection, a sequence of events can progress and ultimately lead to gastric cancer. Treatment of the infection has also been associated with reduced incidence of gastric cancer.[13]Initially, acute inflammation occurs, followed by chronic active pangastritis, then gastric atrophy, intestinal metaplasia, dysplasia, and last, cancer.[6] The chronic inflammatory response causes increased cell turnover that may result in the accumulation of mitotic errors. In addition, reactive oxygen species and reactive nitrogen species released by neutrophils and macrophages cause oxidative stress and DNA damage.[6] Cyclooxygenase 2, cytokines, and interleukins are thought to play a role as well.[14] Cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) are two well-studied virulence factors that have been found in more virulent strains of H pylori.[15] All these factors have been associated with progression to cancer. In a similar fashion, gastric MALT lymphoma arises secondary to recruitment of B cells (stimulated by T cells) that undergo malignant transformation due to genetic mutations.[16]

Currently, noninvasive and invasive testing options are available for H pylori, and a single test is usually sufficient for diagnosis.[17] Noninvasive methods include the urea breath test, fecal antigen test, and serology. The first two can be used to confirm active infection or eradication after treatment. Serologic testing with immunoglobulins A, G, and M is mainly used for epidemiologic studies. Serologic results remain positive after infection and have limited clinical value. The results do have a high negative predictive value, which is useful to exclude the diagnosis in populations with a low prevalence.[18] Of note, the use of PPIs, histamine 2 receptor antagonists (H2RAs), and bismuth-containing antacids can affect testing results and should be discontinued 2 weeks prior to testing.[18]In the urea breath test, the patient ingests a small dose of radiolabeled urea. If active urease is present, the urea will be converted into ammonia and radiolabeled carbon dioxide. The latter is absorbed by the blood, expired through the lungs, and measured from the patient's breath by mass spectrometry.[18] The stool antigen test detects H pylori antigens in stool using polyclonal or monoclonal anti–H pylori antibodies.

Invasive testing includes histology, culture, enzyme-linked immunosorbent assay (ELISA) antibody testing of tissue, and the rapid urease (Campylobacter-like organism [CLO]) test. PPIs should be discontinued 2 weeks before testing to avoid false-negative results; however, H2RAs do not affect microscopic detection. Antibiotics should also be avoided for 4 weeks before the study. After biopsies are obtained through esophagogastroduodenoscopy, H pylori can be detected with hematoxylin and eosin staining and less commonly with Giemsa staining, immunohistochemical staining (Figure 3 and Figure 4), and direct ELISA antibody testing.[19] Culture is typically reserved for cases that are refractory to treatment to determine antibiotic resistance. Molecular-based testing such as polymerase chain reaction is rarely used or available in clinical practice. The rapid urease (CLO) test consists of placing a biopsy sample in a medium with urea and a pH indicator. The presence of urease turns urea into carbon dioxide and ammonia, increasing the pH and causing a change in color in the pH indicator.[19]

Figure 3.

Figure 4.


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